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- W2891366641 abstract "A number of autoimmunity-associated MHC class II proteins interact only weakly with the invariant chain–derived class II–associated invariant chain peptide (CLIP). CLIP dissociates rapidly from I-Ag7 even in the absence of DM, and this property is related to the type 1 diabetes–associated β57 polymorphism. We generated knock-in non-obese diabetic (NOD) mice with a single amino acid change in the CLIP segment of the invariant chain in order to moderately slow CLIP dissociation from I-Ag7. These knock-in mice had a significantly reduced incidence of spontaneous type 1 diabetes and diminished islet infiltration by CD4 T cells, in particular T cells specific for fusion peptides generated by covalent linkage of proteolytic fragments within β cell secretory granules. Rapid CLIP dissociation enhanced the presentation of such extracellular peptides, thus bypassing the conventional MHC class II antigen-processing pathway. Autoimmunity-associated MHC class II polymorphisms therefore not only modify binding of self-peptides, but also alter the biochemistry of peptide acquisition." @default.
- W2891366641 created "2018-09-27" @default.
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- W2891366641 date "2018-09-05" @default.
- W2891366641 modified "2023-10-09" @default.
- W2891366641 title "Rapid CLIP dissociation from MHC II promotes an unusual antigen presentation pathway in autoimmunity" @default.
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- W2891366641 doi "https://doi.org/10.1084/jem.20180300" @default.
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